一氧化氮(NO)是细胞通讯中的重要分子,在许多生物过程中也起着重要作用。鉴于NO在面神经损伤后神经变性和再生中的双重作用,我们试图通过系统的文献综述更深入地研究它的作用。使用SCOPUS的文献的全面回顾,PubMed,科克伦图书馆,EMBASE,和GoogleScholar数据库用于评估NO在面神经损伤后神经变性和再生中的诱导和作用。从最终审查的20篇论文中,主要发现是神经元型一氧化氮合酶(nNOS),内皮型一氧化氮合酶(eNOS),和诱导一氧化氮合酶(iNOS)的增加或减少取决于面神经损伤的方法,受损区域,收获面积,和动物年龄,并与面神经的变性和再生有关。对大鼠和小鼠进行的研究表明,NO,nNOS,eNOS,iNOS在神经再生和变性中起重要作用。然而,神经损伤与NO之间的关系不能通过简单的因果关系来定义。相反,NOS的参与取决于神经细胞的类型,NO的来源,定时,和表达式的位置,目标动物的年龄,和靠近脑干的损伤位置。因此,nNOS,eNOS,iNOS的表达水平和功能可能有显著差异。
Nitric oxide (NO) is an important molecule in cell communication that also plays an important role in many biological processes. Given the dual role of NO in
nerve degeneration and regeneration after facial
nerve injury, we sought to delve deeper into its role through a systematic literature review. A comprehensive review of the literature employing SCOPUS, PubMed, Cochrane Library, EMBASE, and Google Scholar databases was conducted to evaluate the induction and role of NO in neurodegeneration and regeneration after facial
nerve injury. From the 20 papers ultimately reviewed, the central findings were that neuronal nitric oxide synthase(nNOS), endothelial nitric oxide synthase (eNOS), and induced nitric oxide synthase (iNOS) increased or decreased depending on the method of facial
nerve damage, damaged area, harvested area, and animal age, and were correlated with degeneration and regeneration of the facial
nerve. Research conducted on rats and mice demonstrated that NO, nNOS, eNOS, and iNOS play significant roles in nerve regeneration and degeneration. However, the relationship between nerve damage and NO could not be defined by a simple causal relationship. Instead, the involvement of NOS depends on the type of
nerve cell, source of NO, timing, and location of expression, age of the target animal, and proximity of the damage location to the brainstem. Consequently, nNOS, eNOS, and iNOS expression levels and functions may vary significantly.